While mechanical loading is essential for articular cartilage homeostasis, it also plays a central role in the etiology of osteoarthritis. The mechanotransduction events underlying these dual effects, however, remain unclear. Previously, we have shown that lethal amounts of reactive oxygen species (ROS) were liberated from mitochondrial complex 1 in response to a mechanical insult. The sensitivity of this response to an actin polymerase inhibitor, cytochalasin B, indicated a link between ROS release and cytoskeletal distortion caused by excessive compressive strain. It did not, however, rule out the possibility that ROS may also mediate the beneficial effects of normal stresses that induce lower tissue strains required for proper homeostasis. If this possibility is true, one would expect the amount of ROS released in loaded cartilage to be positively correlated with the level of strain, and ROS should only reach lethal levels under super-physiological deformations. To test this hypothesis, full cartilage tissue strains were measured in cartilage explants subjected to static normal stresses of 0, 0.1, 0.25, 0.5, and1.0 MPa. After compression, the percentage of ROS-producing cells was measured using the oxidation-sensitive fluorescent probe, dihydroethidium, and confocal microscopy. In support of our theory, the percentage of fluorescing cells increased linearly with increasing strains (0-75%, r2 = 0.8, p < 0.05). Additionally, hydrostatic stress, which causes minimal tissue strain, induced minimal ROS release. In terms of cell viability, cartilage explants compressed with strains >40% experienced substantial cell death, while explants with strains

Data from the McMaster Occupational Biomechanics Laboratory were consolidated to evaluate overall trends relating to tissue motion and blood flow in the carpal tunnel. Regarding tissue motion, displacements of the flexor digitorum superficialis (FDS) tendon and its subsynovial connective tissue (SSCT) were found to decrease with greater movement speed and a flexed wrist posture. Notably, changes to shear outcomes including relative tendon-SSCT displacement, the shear strain index (SSI), and maximum velocity ratio (MVR) demonstrate that greater movement speed contributes to SSCT damage according to the shear strain mechanism of injury theorised to promote carpal tunnel syndrome (CTS). Median nerve blood flow was also found to be implicated by wrist flexion, and appeared to decrease with greater CTS severity status. Finally, induced blood flow alteration of the carpal tunnel was found to elicit a median nerve blood flow response similar to the level found in CTS subjects, confirming its effectiveness as an intervention to study tissue motion in a CTS-like state. The influence of altered blood flow on tissue motion was differential, where the higher supradiastolic condition altered FDS displacement, and the lower subdiastolic condition affected SSCT displacement and SSI. These findings provide valuable evidence for changes in median nerve blood flow—and by extension, the local fluid environment within the carpal tunnel—not only being a consequence of SSCT fibrosis characteristic of CTS, but potentially also acting as a cause for said changes in carpal tunnel tissue motion. / Thesis / Master of Science in Kinesiology / This thesis aimed to evaluate and summarize key findings from the McMaster Occupational Biomechanics Laboratory relating to tissue motion and blood flow in the carpal tunnel. Performing repetitive finger movements faster and with a flexed wrist posture were found to decrease the distance travelled of the underlying finger tendon. Blood flow of the median nerve, which is implicated in carpal tunnel syndrome (CTS), is higher with forceful exertion and flexed wrist posture, and lower with greater severity of CTS. Finally, altering blood flow to the carpal tunnel was found to create a CTS-like environment, affected tissue motion in the carpal tunnel, and promoted movement disparity between these tissues that is associated with injury. This suggests that fluid/blood flow changes affecting the carpal tunnel is a plausible mechanism for increasing the likelihood of developing CTS.

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